Critical Reviews™ in Eukaryotic Gene Expression

ISSN for PRINT: 1045-4403

For Online Access

Best Paper Award Selection - Editorial Board Site

2002, Volume12

Issue 1

88 pages

DOI: 10.1615/CritRevEukaryotGeneExpr.v12.i1

Issue price - $169.00

James F. Whitfield
Institute for Biological Sciences, National Research Council of Canada, Bldg. M-54, Montreal Road Campus, Ottawa, ON, K1A 0R6, Canada

Paul Morley
Institute for Biological Sciences, National Research Council of Canada, Bldg. M-54, Montreal Road Campus, Ottawa, ON, K1A 0R6, Canada

Gordon E. Willick
Institute for Biological Sciences, National Research Council of Canada, Bldg. M-54, Montreal Road Campus, Ottawa, ON, K1A 0R6, Canada

There is a need for anabolic drugs that can stimulate bone growth, improve bone microarchitecture, accelerate fracture healing and thus restore bone strength to oteoporotics. The anabolic agents currently leading the way to the clinic are the parathroid hormone (PTH) and some of its adenylyl cyclase-stimulating fragments. Here we discuss what is known about the genes and their products that are stimulated by PTHR1 receptor signals and in four ways cause a large accumulation of bone-building osteoblasts. We will also discuss the currently controversial anabolic activity of the cholesterol-lowering statins and outline a possible mechanism by which they might stimulate BMP-2 expession and bone growth. Finally, we will present the growing evdence for the body’s “fat-o-stat” cytokine—leptin—indirectly restraining bone growth via a hypothalamic factor and at the same serving as a local autocrine/paracrine stimulator of osteoblast activity via IGF-I and an inhibitor of osteoclast generation by stimulating osteoblastic cells’ antiosteoclast OPG (osteoprotegerin) expression and reducing their proosteoclast RANKL expression.

DOI: 10.1615/CritRevEukaryotGeneExpr.v12.i1.20 Download article, 30 pages

Article price - $35.00

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